Moreover, the collaboration of these distinct axes in regulation of cell survival via XIAP and Bcl-xL in NSCLC is consistent with our recent study of another epithelia-origin cancer (Xu et al., 2017), further supporting the notion that co-targeting of FAK and c-MYC represents a line of synthetic lethal inhibition in human epithelia-origin cancers, regardless of genomic status of integrin-FAK axis and c-Myc and context of oncogenic activation. This evidence concerns the gene BCL2L1 and cancer.